The sympathetic nervous system (SNS) plays a signficant role in the development and maintenance of chronic and stress-induced arterial hypertension. Although the specific contribution of the SNS to hypertension is unclear, evidence is reviewed that: (a) the SNS exerts peripheral control over those vascular beds regulating both arterial blood pressure and circulatory-assisted heat dissipation, and (b) certain brain mechanisms serve to integrate differentiated patterns of sympathetic discharge of which vasomotor components form a part. This apparent link between those mechanisms controlling blood pressure and those controlling circulatory-assisted heat dissipation is supported by the investigator's studies demonstrating that the adult Spontaneously Hypertensive Rat (SHR) is characterized by an elevation in thermoregulatory "set-point". If the peripheral vascular beds operating in chronic hypertension are linked, centrally or peripherally, to circulatory-assisted heat dissipation then many of the behavioral and/or physiological responses observed in the adult SHR will occur; (1) simultaneously with the onset of hypertension in the maturing SHR, and (2) in other models of chronic hypertension associated with SNS dysfunction. Accordingly, two series of studies have been proposed that will examine the relationship between the onset of Spontaneous (Series I) and metacorticoid (DOCA-salt) (Series II) hypertension in rats on the animals' ability to physiologically or behaviorally sustain an adequate body temperature under different thermal challenges. The objective will be to: (1) clarify the extent to which thermoregulatory abnormalities consitute a basic syndrome accompanying chronic hypertension, and (2) eventually, to bring together several lines of behavioral, cardiovascular, and neuropharmacological research to characterize the role of the central nervous system in the pathogenesis of experimental and genetic forms of arterial hypertension.